Pigmentary glaucoma is caused by an overwhelming of the trabecular meshwork by pigment that originates from the posterior surface of the iris. Recent investigations by the proposed principal investigator suggested that the cause of the loss of pigment is a mechanical rubbing between the posterior surface of the iris and anterior packets of zonules in predisposed eyes. The study indicated that when the peripheral iris was flat, contact was unlikely. In the laboratory, further study of the pathophysiology of pigmentary glaucoma will be conducted with constant pressure perfusion studies with human pigment infusion into human enucleated eyes. These studies will be correlated with studies to create an animal model for pigmentary glaucoma in rhesus monkeys. The role of phagocytosis in the endothelial cells lining the trabecular meshwork in the creation and cure of secondary and primary open angle glaucoma is poorly understood. To this point, no one has evaluated the possible therapeutic effect of macrophages, injected into living eyes, upon these glaucomas. If a successful animal model for pigmentary glaucoma can be established, macrophages will be injected into the anterior chambers of these living eyes to determine if there is a beneficial effect.